Esmolol antagonist

Class II drugs are classical (3-adrenoceptor antagonists such as propranolol, atenolol, metoprolol or the short-acting substance esmolol. These drugs reduce sinus rate, exert negative inotropic effects and slow atrioventricular conduction. Automaticity, membrane responsiveness and effective refractory period of Purkinje fibres are also reduced. The typical extracardiac side effects are due to (3-adrenoceptor blockade in other organs and include bronchospasm, hypoglycemia, increase in peripheral vascular resistance, depressions, nausea and impotence. 

Esmolol hydrochloride is a competitive p-adrenergic receptor antagonist it is selective for pT adrenoceptors. In contrast to pindolol, esmolol has little intrinsic sympathomimetic activity, and it differs from propranolol in that it lacks membrane stabilizing activity Of all of the p-adrenergic blocking drugs, this compound has the shortest duration of action because it is an ester, it is hydrolyzed rapidly by plasma esterases and must be used by the intravenous route Esmolol is approved only for the treatment of supraventricular arrhythmias... 

Esmolol is an ultra-short-acting relatively 31-selective 3-adrenoceptor antagonist with an elimination half-life of about 9 min. After intravenous administration it is rapidly hydrolysed by non-specific esterases in the blood and tissues to a carboxylic acid metabolite. Following an intravenous infusion its haemodynamic effects are short lasting and disappear within 20-30 min. The main indication in the perioperative period is to treat tachycardia. 

Class II drugs are the p-adrenoceptor antagonists that suppress the sympathetic modulation of the heart action. They are used in the therapy of sinus tachycardia, supraventricular paroxysmal tachycardia and ventricular extra-systoles. Because of its rapid onset and short duration of action, esmolol is the preferred drug in this class for intra-operative use. 

If a (3-adrenoceptor antagonist is administered prior to sufficient ol-radrenoceptor blockade, a hypertensive episode may be precipitated with cardiac failure and pulmonary oedema. Most intravenous anaesthetic agents have been used safely, but ketamine is contraindicated. Sodium nitroprusside can be used to achieve arteriolar dilation. Esmolol, a pi-selective antagonist with very short duration of action, is administered intravenously to prevent cardiac arrhythmias intra-operatively. After tumour removal, volume administration should be aggressive to maintain haemodynamic stability, and a noradrenaline infusion may be required. 

Esmolol is an ultra-short-acting Bit-selective adrenoceptor antagonist. The structure of esmolol contains an ester linkage ... 

C. Acebutolol, atenolol, metoprolol and esmolol selective p1 antagonists... 

Esmolol is a betai-selective adrenoceptor antagonist with an extremely short half-life (about 10 minutes), because of extensive metabolism by esterases in blood, liver, and other tissues. 

Atenolol is a selective Pi adrenoceptor antagonist that undergoes almost no hepatic metabolism. As such, the drug is favored for oral administration to other species but it has not been utilized clinically in the horse. Similarly, esmolol, an ultra-short acting Pi adrenoceptor-blocking drug that undergoes plasma esterification, has not yet been used in the horse. Esmolol is used in other species for the treatment of supraventricular tachycardias. 

The short duration of action of esmolol is the Ksult i> rapid hydrolysis of its e.sler functionality by cslciuscsprcKiii in erythrocytes (Fig. 16-10). The resultant carboxylic so is an extremely weak P antagonist that docs not. ippctrii exhibit clinically significant effects. The acid mclabnlileb an elimination half-life of 3 to 4 hours and is excreted pr-marily by the kidneys. 

Antagonists with similar affinity for p,-adrenoceptor and P2-adrenoceptors include nadolol, oxprenolol, propranolol and timolol whereas acebutolol, atenolol, esmolol and metoprolol show some Pi -adrenoceptor selectivity and butoxaminc is pz-adrenoceptor preferring. Labetolol, in the racemic form used in medicine, acts as both a P-adrenoceptor and an a-adrenoceptor antagonist, though these activities reside in different isomers. Further factors determining the uses of individual agents include variations... 

Celectol celiprolol esmolol. celiprolol [ban, inn, usan] (Celectol ) is a P-adrenoceftor antagonist, which is relatively water-soluble. It can be used therapeutically in ANTlANGiNAL and hypertensive treatment, celiprolol hydrochloride celiprolol. 

Esmeron rocuronium bromide, esmolol [BAN, inn] (esmolol hydrochloride [usan] Brevibloc Celectol ) is a P-adrenoceptor antagonist, which is relatively water-soluble. Therapeutically, it can be used as an antiarrhythmic to control supraventricular tachyarrhythmias, as an antihypertensive and antiglaucoma treatment. 

Mixed a antagonists phenoxybenzamine, phentolamine Pt (cardioselective) antagonists acebutolol, atenolol, esmolol, metoprolol Pj P2 (nonselective) pindolol, propranolol, timolol Oj and P antagonists carvedilol, labetalol... 

Esmolol (Brevibloc, others) is a Pi-selective antagonist with a very short duration of action. It has little if any intrinsic sympathomimetic activity, and it lacks membrane-stabilizing actions. Esmolol is administered intravenonsly and is nsed when P-blockade of short dnration is desired, or in critically ill patients in whom adverse effects of bradycardia, heart failure, or hypotension may necessitate rapid withdrawal of the drug. 

These drugs decrease calcium flux in the AV node, and decrease the excitability of cardiac tissue. This class includes Preceptor antagonists (e.g., esmolol) and pan-beta receptor antagonists (e.g., propranolol). 

Esmolol is a beta antagonist with a short half-life. Thus, it is most useful in the therapy of acute arrhythmias, and as an adjunct to surgical procedures. 

Mitrovic. V. Oehm, E. Thormann. J. Pitschner. H. Haberbosch. W. Comparison of the potassium channel blocker tedisamil with the 3-adrenoceptor blocker esmolol and the calcium antagonist gallopamil in patients with coronary artery disease. Clin. Cardiol. 1998. 27, 492-502. 

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